切换至 "中华医学电子期刊资源库"

中华神经创伤外科电子杂志 ›› 2020, Vol. 06 ›› Issue (06) : 360 -363. doi: 10.3877/cma.j.issn.2095-9141.2020.06.008

所属专题: 文献

基础研究

右美托咪啶在南海近滩海水条件下对开放性颅脑损伤的抗炎和脑保护作用
冯龙1, 尹一恒2, 郑杨睿3, 汤浩3, 段明达1, 曹江北4, 袁维秀1, 张宏4, 余新光2,()   
  1. 1. 572000 三亚,解放军总医院海南医院麻醉科
    2. 100853 北京,解放军总医院第一医学中心神经外科
    3. 572000 三亚,解放军总医院海南医院神经外科
    4. 100853 北京,解放军总医院第一医学中心麻醉手术中心
  • 收稿日期:2020-10-26 出版日期:2020-12-15
  • 通信作者: 余新光
  • 基金资助:
    三亚市医疗卫生科技创新项目(2018YW16); 军队十三五课题(AWS15J001)

Dexmedetomidine has anti-inflammatory and brain protective effects after open craniocerebral injury in the South China Sea near the beach

Long Feng1, Yiheng Yin2, Yangrui Zheng3, Hao Tang3, Mingda Duan1, Jiangbei Cao4, Weixiu Yuan1, Hong Zhang4, Xinguang Yu2,()   

  1. 1. Department of Anesthesiology, Hainan Hospital, General Hospital of Chinese PLA, Sanya 572000, China
    2. Department of Neurosurgery, First Medical Center, General Hospital of Chinese PLA, Beijing 100853, China
    3. Department of Neurosurgery, Hainan Hospital, General Hospital of Chinese PLA, Sanya 572000, China
    4. Anesthesia Center Surgery, First Medical Center, General Hospital of Chinese PLA, Beijing 100853, China
  • Received:2020-10-26 Published:2020-12-15
  • Corresponding author: Xinguang Yu
  • About author:
    Corresponding author: Yu Xinguang, Email:
引用本文:

冯龙, 尹一恒, 郑杨睿, 汤浩, 段明达, 曹江北, 袁维秀, 张宏, 余新光. 右美托咪啶在南海近滩海水条件下对开放性颅脑损伤的抗炎和脑保护作用[J]. 中华神经创伤外科电子杂志, 2020, 06(06): 360-363.

Long Feng, Yiheng Yin, Yangrui Zheng, Hao Tang, Mingda Duan, Jiangbei Cao, Weixiu Yuan, Hong Zhang, Xinguang Yu. Dexmedetomidine has anti-inflammatory and brain protective effects after open craniocerebral injury in the South China Sea near the beach[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2020, 06(06): 360-363.

目的

研究海战开放性脑损伤后使用右美托咪啶是否具有抗炎脑保护作用。

方法

选择新西兰兔12只,随机分为右美托咪啶组(Dex组)和生理盐水对照组(Con组),每组各6只。在地西泮麻醉下建立创伤性脑损伤模型。实验兔脑开放伤口经南海海水冲洗60 min后,Dex组实验兔腹腔注射50 mg/kg盐酸右美托咪啶,Con组给予相同剂量生理盐水。给药缝合好伤口后继续饲养48 h处死实验兔,取脑组织标本做HE染色。采外周血通过ELISA试剂盒检测白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)及中枢神经特异性蛋白(S100-β)指标水平变化。

结果

Con组创伤性脑细胞水肿主要表现为神经元和神经胶质细胞胞体明显肿胀,原有的椎体形状无法清晰辨认,细胞核浓染色,且出现细胞核周围环形低染甚至是空白染色区;而Dex组可明显改善以上组织细胞损伤和水肿的变化。ELISA法检测结果显示,和Con组相比,Dex组IL-1β、TNF-α和S100-β的水平明显降低,差异有统计学意义(P<0.05),而2组的IL-6水平变化比较差异无统计学意义(P>0.05)。

结论

颅脑开放性损伤后经南海近滩海水浸泡后给予右美托咪啶具有抗炎和脑保护作用。

Objective

To investigate whether dexmedetomidine has anti-inflammatory brain protective effect after open brain injury in naval warfare.

Methods

Twelve New Zealand rabbits were selected and randomly divided into dexmedetomidine group (Dex group) and control group (Con group), with six rabbits in each group. The model of traumatic brain injury was established under diazepam anesthesia. The open wound of the experimental rabbit brain was washed with seawater in the South China Sea for 60 min. The rabbits in the Dex group were injected intraperitoneally with 50 mg/kg dexmedetomidine, and the Con group was given the same dose of normal saline. After administration of the sutured wound, the rabbits were sacrificed for 48 h. The brain tissue samples were taken for HE staining. Peripheral blood was collected to detect changes in interleukin 1β (IL-1β), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and S100-β indicators by ELISA kits.

Results

The traumatic brain cell edema in the Con group was mainly manifested by the obvious swelling of neurons and glial cell bodies, the original shape of the vertebral body could not be clearly identified, the nucleus was strongly stained, and there was a circular low staining or even a blank staining area around the nucleus; However, Dex group can significantly improve the above changes in all neurons damage and edema. The results of ELISA showed that compared with the Con group, the levels of IL-1β, TNF-α, and S100-β in the Dex group were significantly reduced, and the differences between the groups were statistically significant (P<0.05); While, there was no significant difference in IL-6 level between the two groups (P>0.05).

Conclusion

Anti-inflammatory and brain-protective effects of dexmedetomidine after seawater immersion in the South China Sea after open brain injury.

图1 创伤性脑损伤后实验兔脑组织HE染色结果
表1 2组实验兔脑创伤后48 h后炎症因子水平的比较
[1]
Hyder AA, Wunderlich CA, Puvanachandra P, et al. The impact of traumatic brain injuries: a global perspective[J]. Neuro Rehabilitation, 2007, 22(5): 341-353.
[2]
Lei J, Gao G, Jiang J. Acute traumatic brain injury: is current management evidence based? An empirical analysis of systematic reviews[J]. J Neurotrauma, 2013, 30(7): 529-537.
[3]
Chen YC, Smith DH, Meaney DF. In-vitro approaches for studying blast-induced traumatic brain injury[J]. J Neurotrauma, 2009, 26(6): 861-876.
[4]
Nelson LE, Lu J, Guo T, et al. The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects[J]. Anesthesiology, 2003, 98(2): 428-436.
[5]
Farrell D, Bendo AA. Perioperative management of severe traumatic brain injury: what is new?[J]. Curr Anesthesiol Rep, 2018, 8(3): 279-289.
[6]
Feeney DM, Boyeson MG, Linn RT, et al. Responses to cortical injury: I. Methodology and local effects of contusions in the rat[J]. Brain Res, 1981, 211(1): 67-77.
[7]
夏照帆,马兵.现代战争条件下海战创伤救治的几点思考[J].解放军医学杂志, 2016, 41(12): 973-976.
[8]
吴新文,吴珺.现代海战伤员特点及救治措施[J].人民军医, 2002, 45(6): 315-316.
[9]
Choi HA, Jeon SB, Samuel S, et al. Paroxysmal sympathetic hyperactivity after acute brain injury[J]. Curr Neurol Neurosci Rep, 2013, 13(8): 370.
[10]
Du J, Xiao K, Li L, et al. Temporal and spatial diversity of bacterial communities in coastal waters of the South china sea[J]. PLoS One, 2013, 8(6): e66968.
[11]
Baguley IJ, Perkes IE, Fernandez-Ortega JF, et al. Paroxysmal sympathetic hyperactivity after acquired brain injury: consensus on conceptual definition, nomenclature, and diagnostic criteria[J]. J Neurotrauma, 2014, 31(17): 1515-1520.
[12]
Flower O, Hellings S. Sedation in traumatic brain injury[J]. Emerg Med Int, 2012, 2012: 637171.
[13]
Lump D, Moyer M. Paroxysmal sympathetic hyperactivity after severe brain injury[J]. Curr Neurol Neurosci Rep, 2014, 14(11): 494.
[14]
Sshu S, Nag DS, Swain A, et al. Biochemical changes in the injured brain[J]. World J Biol Chem, 2017, 8(1): 21-31.
[15]
Taupin V, Toulmond S, Serrano A, et al. Increase in IL-6, IL-1 and TNF levels in rat brain following traumatic lesion. Influence of pre- and post-traumatic treatment with Ro5 4864, a peripheral-type (p site) benzodiazepine ligand[J]. J Neuroimmunol, 1993, 42(2): 177-185.
[16]
Ding M, Chen Y, Luan H, et al. Dexmedetomidine reduces inflammation in traumatic brain injury by regulating the inflammatory responses of macrophages and splenocytes[J]. Exp Ther Med, 2019, 18(3): 2323-2331.
[17]
Singhal A, Baker AJ, Hare GM, et al. Association between cerebrospinal fluid interleukin-6 concentrations and outcome after severe human traumatic brain injury[J]. J Neurotrauma, 2002, 19(8): 929-937.
[18]
Pleines UE, Morganti-Kossmann MC, Rancan M, et al. S-100 beta reflects the extent of injury and outcome, whereas neuronal specific enolase is a better indicator of neuroinflammation in patients with severe traumatic brain injury[J]. J Neurotrauma, 2001, 18(5): 491-498.
[19]
Li F, Wang X, Zhang Z, et al. Dexmedetomidine attenuates neuroinflammatory-induced apoptosis after traumatic brain injury via Nrf2 signaling pathway[J]. Ann Clin Transl Neurol, 2019, 6(9): 1825-1835.
[20]
Shen M, Wang S, Wen X, et al. Dexmedetomidine exerts neuroprotective effect via the activation of the PI3K/Akt/mTOR signaling pathway in rats with traumatic brain injury[J]. Biomed Pharmacother, 2017, 95: 885-893.
[21]
Schoeler M, Loetscher PD, Rossaint R, et al. Dexmedetomidine is neuroprotective in an in vitro model for traumatic brain injury[J]. BMC Neurol, 2012, 12(11): 20.
[22]
Dahmani S, Rouelle D, Gressens P, et al. Characterization of the postconditioning effect of dexmedetomidine in mouse organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation[J]. Anesthesiology, 2010, 112(2): 373-383.
[23]
Wang J, Lei B, Popp S, et al. Sevoflurane immediate preconditioning alters hypoxic membrane potential changes in rat hippocampal slices and improves recovery of CA1 pyramidal cells after hypoxia and global cerebral ischemia[J]. Neuroscience, 2007, 145(3): 1097-1107.
[1] 阿迪莱·阿卜杜热西提, 费奥, 邢晓雯, 谢胜强, 张睿, 兰晓娟, 程岗. 三种模拟创伤性脑损伤体外细胞模型的损伤特征比较[J]. 中华神经创伤外科电子杂志, 2023, 09(02): 69-75.
[2] 王建鹏, 廖勇仕, 丁文聪, 李冲, 陈锐. lncRNA在创伤性脑损伤中的研究进展[J]. 中华神经创伤外科电子杂志, 2022, 08(06): 365-370.
[3] 崔刚, 王德亮, 付茂武, 田璧铭, 王莹, 段虎斌. 创伤性脑损伤后鼠脑内RHO/ROCK信号通路与神经炎症反应及病理性损伤关系的研究[J]. 中华神经创伤外科电子杂志, 2022, 08(06): 324-328.
[4] 傅世龙, 王国锋, 侯鹏伟, 袁邦清, 魏梁锋, 王守森. 颅脑创伤患者术后再次开颅清除对侧血肿的影响因素分析[J]. 中华神经创伤外科电子杂志, 2022, 08(05): 287-292.
[5] 程俊凯, 罗耀文, 李娟, 张磊, 杨淑涵, 王彦刚. 重复经颅磁刺激上调DJ-1表达改善小鼠创伤性脑损伤后功能障碍的研究[J]. 中华神经创伤外科电子杂志, 2022, 08(05): 261-268.
[6] 崔刚, 肖友朝, 王欢, 田璧铭, 王莹, 段虎斌. RHO/ROCK信号通路对创伤性脑损伤后颅内神经系统微环境的影响[J]. 中华神经创伤外科电子杂志, 2022, 08(04): 204-208.
[7] 王鸿, 高俊宏, 卢青, 刘进仁, 范小琳, 李亮, 马宁, 王琪. 基于CiteSpace的创伤性脑损伤研究文献计量学分析[J]. 中华神经创伤外科电子杂志, 2022, 08(03): 141-149.
[8] 齐洪武, 刘岩松, 曾维俊, 张立钊, 郭洪均, 刘清石. 儿童创伤性脑损伤的研究进展[J]. 中华神经创伤外科电子杂志, 2022, 08(02): 121-124.
[9] 毕万达, 刘阳珷玥, 戴双双. 载脂蛋白E在创伤性脑损伤中作用及机制的研究进展[J]. 中华神经创伤外科电子杂志, 2022, 08(01): 51-55.
[10] 余鹏飞, 麦兴进, 符树强, 苏保寿, 吴益敏, 喻闻庆. 血清sTREM-1、IL-12及IL-33水平对创伤性脑损伤严重程度和预后评估的价值[J]. 中华神经创伤外科电子杂志, 2022, 08(01): 18-22.
[11] 胡霁云, 谢树才, 张丽娜. S100钙结合蛋白B与重症神经研究进展[J]. 中华重症医学电子杂志, 2023, 09(03): 298-303.
[12] 杨丽婷, 潘东峰, 白雪, 张玲, 陈梦飞. 目标体温管理对心脏骤停患者脑保护作用的研究进展[J]. 中华脑科疾病与康复杂志(电子版), 2022, 12(05): 310-314.
[13] 沈丘月, 侯新琳. n-3多不饱和脂肪酸脑保护机制研究进展[J]. 中华临床医师杂志(电子版), 2023, 17(04): 471-478.
[14] 史绿儿, 任奇, 沈杭霞. 右美托咪啶对老年患者心脏手术疗效影响的Meta分析[J]. 中华老年病研究电子杂志, 2023, 10(01): 34-40.
[15] 潘鑫, 王华, 王忻, 顾慧, 王超. 院前右美托咪啶与丙泊酚对需要机械通气的成人危重症患者镇静效果的比较[J]. 中华卫生应急电子杂志, 2022, 08(06): 331-334.
阅读次数
全文


摘要